Stages of Labor

Labor is considered “normal” when the woman is at or near term, no

complications exist, as single fetus presents by vertex and labor is completed within

24 hrs. The course of labor has 4 stages:

First Stage of Labor

The first stage of labor is the longest. There are three phases within the first

stage: Early or latent phase, Active phase and Transition phase. At the end of the

first stage, the cervix is dilated to 10 centimeters. In mothers having their first child,

this stage usually lasts 12 to 16 hours. For women having second or subsequent

children, the first stage lasts around 6-7 hours.

Early/Latent

During the early or latent phase, the cervix dilates to 4 centimeters.

The duration of the first phase is the longest, averaging around 8 hours. Your

contractions may be irregular, progressing to rhythmic and methodical. The

pain felt at this early stage may be similar to menstrual pain: aching, fullness,

cramping and backache. You will still be able to walk. Walking is usually more

comfortable than sitting. Most women spend these hours at home, or they

may be checked at the hospital and sent home until labor becomes more

active. You may feel eager, excited and social. It is important that you

conserve your energy for the work of labor.

Active

Active labor is marked by regular contractions that become longer,

stronger and closer together over time. Most providers recommend that you

go to the hospital when your contractions are five minutes apart, lasting more

then 60 seconds for at least an hour.

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If you have had previous deliveries, the active phase of labor can proceed

more quickly. When you are in active labor, you will be concentrating on the

task at hand, and will not feel like doing anything else. Contractions are

growing stronger, longer and closer together. Contractions will be about 3-4

minutes apart, lasting 40 to 60 seconds. You may have a tightening feeling in

your pubic area and increasing pressure in your back. If you have learned

breathing techniques, begin using them now. Pain medication is often given

at this stage. If you have chosen to have an epidural anesthetic, it is usually

given at this stage.

Transition

Transition is the most difficult phase of labor, and fortunately, the

shortest, lasting from 30 minutes to two hours. The cervix is opening the last

few centimeters, from 7 to 10 centimeters. The pain may be intense, as the

cervix stretches and the baby descends into the birth canal. All of your energy

is concentrated on doing the work of labor. At the end of transition, you may

feel a strong urge to push the baby out. The baby is ready to be born.

Second Stage of Labor

The second stage begins from the time the cervix is fully dilated(10 cm) until

the baby is born. This stage of labor lasts anywhere from one contraction up to two

hours. The baby's head stretches your vagina and perineum (the skin between the

vagina and rectum). This may cause a burning sensation. Some women may feel as

if they are having a bowel movement, and feel the urge to push, or bear down. The

labor nurse or physician will tell you when it is time to push. It is important that you

not push until instructed. Pushing too early will cause the cervix to become

edematous, or swollen. "Crowning" occurs as the widest part of the head appears at

the vaginal opening. In the next few pushes, the baby is born. Mucous and amniotic

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fluid will be removed from the baby's mouth and nose with a bulb syringe. The baby

will take its first breath, and may begin to cry. Immediately after birth, the baby is still

connected to the placenta by the umbilical cord. The cord is clamped and cut.

Third Stage of Labor

The third stage of labor, or the placental site, begins with the birth of the infant

and ends with the delivery of the placenta. Two separate phases are involved:

placental separation and placental separation and placental expulsion. Signs of

placental separation includes: calkin’s sign, uterus becomes mobile, sudden gushing

of blood and lengthening of umbilical cord. The types of placental delivery or

presentation includes: schultze’s mechanism, which is the shiny “clean” side first

bluish side and duncan’s mechanism, appears to be rough, ”dirty”, reddish maternal

side out first.

After birth of the infant, the uterus can be palpated as a firm, round mass just

inferior to the level of the umbilicus. After few minutes of rest, uterine contractions

begin again, and the organ assumes a discoid shape. It retains this new shape until

the placenta has separated, approximately 5 minutes after the birth of the infant.

Fourth Stage of Labor

This stage is really more about getting back to normal than anything else --

the hour or two after delivery when the tone of the uterus is established and the

uterus contracts down again expelling any remaining contents. These contractions

are hastened by breast-feeding, which stimulates production of the hormone

oxytocin. Your blood pressure, temperature and heart rate will stabilize in much the

same way a marathon runners does: a little at a time during the hour after the

placenta is delivered. Contractions will cease. Your uterus will harden, doing its job

to tighten around the blood vessels that had supplied the placenta and your baby

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with nutrients. Your midwife or doctor will keep an eye on you, make sure the entire

placenta was expelled and take a look at the umbilical cord. If you had an

episiotomy, this is when you'll get a few sutures.

Postpartal hemorrhage is usually defined as the loss of more than 500 ml of

blood during or after delivery. It is one of the leading causes of maternal mortality.

Hemorrhage may occur early, within the first 24 hr after delivery, or late, up to 28

days postpartum (the end of the puerperium).

Causes of postpartum hemorrhage

4 categories, commonly called "The Four T's":

Trauma from the delivery may tear tissue and vessels leading to significant

postpartum bleeding.

Uterine atony (Tone) refers to the inability of the uterus to contract and may

lead to continuous bleeding. Retained placental tissue and infection may

contribute to uterine atony.

Tissue refers to any cellular debris from the placenta or fetus that may be left

in the uterus, causing the uterus to not contract.

Thrombin refers to some failure of clotting, such as with diseases known as

coagulopathies.

Complications from postpartum hemorrhage include orthostatic hypotension,

anemia, and fatigue, which may make maternal care of the newborn more difficult.

Postpartum anemia increases the risk of postpartum depression. Blood transfusion

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may be necessary and carries associated risks. In the most severe cases,

hemorrhagic shock may lead to anterior pituitary ischemia with delay or failure of

lactation (i.e., postpartum pituitary necrosis).

Tone

Uterine atony is the most common cause of postpartum hemorrhage.

Because hemostasis associated with placental separation depends on myometrial

contraction, atony is treated initially by bimanual uterine compression and massage,

followed by drugs that promote uterine contraction.

Figure 1. Technique of bimanual massage for uterine atony. Bimanual uterine

compression massage is performed by placing one hand in the vagina and pushing

against the body of the uterus while the other hand compresses the fundus from

above through the abdominal wall. The posterior aspect of the uterus is massaged

with the abdominal hand and the anterior aspect with the vaginal hand.

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Uterine Massage. Brisk blood flow after delivery of the placenta should

alert the physician to perform a bimanual examination of the uterus. If the

uterus is soft, massage is performed by placing one hand in the vagina

and pushing against the body of the uterus while the other hand

compresses the fundus from above through the abdominal wall (Figure 1).

The posterior aspect of the uterus is massaged with the abdominal hand

and the anterior aspect with the vaginal hand.

Uterotonic Agents. Uterotonic agents include oxytocin, ergot alkaloids,

and prostaglandins. Oxytocin stimulates the upper segment of the

myometrium to contract rhythmically, which constricts spiral arteries and

decreases blood flow through the uterus. Oxytocin is an effective first-line

treatment for postpartum hemorrhage; 10 international units (IU) should be

injected intramuscularly, or 20 IU in 1 L of saline may be infused at a rate

of 250 mL per hour. As much as 500 mL can be infused over 10 minutes

without complications.

Figure 2. Reduction of uterine inversion (Johnson method). (A) The

protruding fundus is grasped with fingers directed toward the posterior

fornix. (B, C) The uterus is returned to position by pushing it through the

pelvis and into the abdomen with steady pressure towards the umbilicus.

Misoprostol is another prostaglandin that increases uterine tone

and decreases postpartum bleeding. Misoprostol is effective in the

treatment of postpartum hemorrhage, but side effects may limit its use. It

can be administered sublingually, orally, vaginally, and rectally. Higher

peak levels and larger doses are associated with more side effects,

including shivering, pyrexia, and diarrhea.

Trauma

Lacerations and hematomas resulting from birth trauma can cause

significant blood loss that can be lessened by hemostasis and timely repair.

Sutures should be placed if direct pressure does not stop the bleeding.

Hematomas can present as pain or as a change in vital signs

disproportionate to the amount of blood loss. Small hematomas can be managed

with close observation. Patients with persistent signs of volume loss despite fluid

replacement, as well as those with large or enlarging hematomas, require

incision and evacuation of the clot. The involved area should be irrigated and the

bleeding vessels ligated. In patients with diffuse oozing, a layered closure will

help to secure hemostasis and eliminate dead space.

Uterine Inversion. Uterine inversion is rare, occurring in 0.05 percent of

deliveries. Active management of the third stage of labor may reduce the

incidence of uterine inversion. Fundal implantation of the placenta may

lead to inversion; the roles of fundal pressure and undue cord traction are

uncertain. The inverted uterus usually appears as a bluish-gray mass

protruding from the vagina. The Johnson method of reduction begins with

grasping the protruding fundus with the palm of the hand and fingers

directed toward the posterior fornix. The uterus is returned to position by

lifting it up through the pelvis and into the abdomen. Once the uterus is

reverted, uterotonic agents should be given to promote uterine tone and to

prevent recurrence.

Uterine Rupture. Although rare in an unscarred uterus, clinically

significant uterine rupture occurs in 0.6 to 0.7 percent of vaginal births

after cesarean delivery in women with a low transverse or unknown

uterine scar. The risk increases significantly with previous classical

incisions or uterine surgeries, and to a lesser extent with shorter intervals

between pregnancies or a history of multiple cesarean deliveries,

particularly in women with no previous vaginal deliveries. Compared with

spontaneous labor, induction or augmentation increases the rate of uterine

rupture, more so if prostaglandins and oxytocin are used sequentially.

Before delivery, the primary sign of uterine rupture is fetal

bradycardia. Tachycardia or late decelerations can also herald a uterine

rupture, as can vaginal bleeding, abdominal tenderness, maternal

tachycardia, circulatory collapse, or increasing abdominal girth.

Symptomatic uterine rupture requires surgical repair of the defect or

hysterectomy. When detected in the postpartum period, a small

asymptomatic lower uterine segment defect or bloodless dehiscence can

be followed expectantly.

Tissue

Classic signs of placental separation include a small gush of blood with

lengthening of the umbilical cord and a slight rise of the uterus in the pelvis.

Placental delivery can be achieved by use of the Brandt-Andrews maneuver,

which involves applying firm traction on the umbilical cord with one hand while

the other applies suprapubic counterpressure. The mean time from delivery until

placental expulsion is eight to nine minutes. Longer intervals are associated with

an increased risk of postpartum hemorrhage, with rates doubling after 10

minutes. Retained placenta (i.e., failure of the placenta to deliver within 30

minutes after birth) occurs in less than 3 percent of vaginal deliveries. One

management option is to inject the umbilical vein with 20 mL of a solution of 0.9

percent saline and 20 units of oxytocin. This significantly reduces the need for

manual removal of the placenta compared with injecting saline alone.

Figure 3. Brandt-Andrews maneuver for cord traction. Firm traction is

applied to the umbilical cord with one hand while the other applies suprapubic

counterpressure.

Thrombin

Coagulation disorders, a rare cause of postpartum hemorrhage, are

unlikely to respond to the measures described above. Most coagulopathies are

identified before delivery, allowing for advance planning to prevent postpartum

hemorrhage. These disorders include idiopathic thrombocytopenic purpura,

thrombotic thrombocytopenic purpura, von Willebrand's disease, and hemophilia.

Patients also can develop HELLP (hemolysis, elevated liver enzyme levels, and

low platelet levels) syndrome or disseminated intravascular coagulation. Risk

factors for disseminated intravascular coagulation include severe preeclampsia,

amniotic fluid embolism, sepsis, placental abruption, and prolonged retention of

fetal demise. Abruption is associated with cocaine use and hypertensive

disorders. Excessive bleeding can deplete coagulation factors and lead to

consumptive coagulation, which promotes further bleeding. Coagulation defects

should be suspected in patients who have not responded to the usual measures

to treat postpartum hemorrhage, and in those who are not forming blood clots or

are oozing from puncture sites.

Lab Studies

In the antenatal period, a CBC is performed. Findings alert caregivers to

women with anemia and indicate interventions to attempt to improve the

hemoglobin level. Hemoglobin levels below 10-10.5 g/dL have been

associated with adverse pregnancy outcome, and the rare patient with

thrombocytopenia will be identified (Xiong, 2000). Women admitted to

labor and delivery units should have a CBC performed if one has not been

performed recently. All women experiencing antepartum bleeding should

have a CBC.

Blood typing and antibody screening tests may also have been performed

in the antenatal period. If the results are known and no blood group

antibodies were present, then the test may not need to be repeated upon

admission. However, many facilities routinely repeat this test (or at least

draw a sample to be held in the blood bank) in case blood is urgently

needed. The time frame between a request for blood products of various

types and their availability should be known. In a patient at high risk of

PPH, crossmatching of 2-6 U of blood before delivery is prudent.

Examples include previous severe PPH, placenta previa, possible

placenta accreta, multiple previous cesarean deliveries, known

coagulation disorders, or severe thrombocytopenia. The American

Association of Blood Banks currently recommends retesting women at

high risk every 72 hours for the development of antibodies.

Coagulation studies are no longer routinely performed in pregnant women,

including those about to undergo cesarean delivery. Instead, history is

relied on to uncover previous episodes suggesting preexisting hemostasis

disorders.

Placenta Previa is the abnormal implantation of the placenta in the lower

uterine segment, partially or completely covering the internal cervical os.

CLASSSIFICATION:

Total placenta previa – implantation that totally obstructs the cervical os

Partial placenta previa – implantation that occludes a portion of the

cervical os

Marginal placenta previa - placenta edge approaches the cervical os

Low-lying placenta – implantation in the lower rather than in the upper

portion of the uterus

PATHOPHYSIOLOGY AND ETIOLOGY

The cause is unknown.

One possible theory states that the embryo will implant in the lower uterine

segment if the decidua in the uterine fundus is not favorable or delayed

implantation.

About 80% of placenta previa episode occur in multiparas.

Seen more often with history of abortion, cesarean section, uterine

scarring or prior placenta previa.

Age greater than 35 years of age.

Conditions that yield abnormally large placentas such as multifetal

gestation or Rh isoimmunization.

CLINICAL MANIFESTATIONS:

Cardinal sign is painless vaginal bleeding, which usually appears near the

end of the second trimester or later. Bleeding appears without warning.

Initial episode is rarely fatal and usually stops spontaneously, with

subsequent bleeding episodes occurring spontaneously; each episode is

more profuse than the previous one.

Bleeding from placenta may not occur until cervical dilation occurs and the

placenta is loosened from the uterus.

With a complete placenta previa, the bleeding will occur earlier in

pregnancy and be more profuse.

DIAGNOSTIC EVALUATION

Transabdominal ultrasound is the method of choice to show location of the

placenta.

If findings are questionable, transvaginal ultrasound can improve the

accuracy of the diagnosis.

Sterile speculum examination can also confirm placenta previa.

MANAGEMENT

Conservative management with bed rest and hospitalization until fetus is

mature and delivery can be accomplished.

If woman is discharged, she needs availability of immediate transport for

recurrent bleeding.

IV access and at least 2 units of blood should be available at all times.

Continuous maternal and fetal monitoring.

Cesarean section is often indicated if the degree of previa is >30% or if

there is excessive bleeding.

Vaginal delivery may sometimes be attempted in a marginal previa without

active bleeding.

A pediatric specialty team may be needed at delivery due to prematurity

and other neonatal complications.

COMPLICATIONS

Fetal mortality resulting from hypoxia in utero and prematurity.

Immediate hemorrhage, with possible shock and maternal death.

Postpartum hemorrhage resulting from decreased contractility of uterine

muscle.

NURSING ASSESSMENT

Determine the amount and type of bleeding; also, review any history of

bleeding throughout this pregnancy.

Inquire as to the presence or absence of pain in association with the

bleeding.

Record maternal and fetal vital signs.

Palpate for the presence of uterine contractions.

Evaluate laboratory data ion hemoglobin and hematocrit status.

NURSING DIAGNOSIS INTERVENTION RATIONALE

Altered Tissue Perfusion, Placental, related to excessive bleeding causing fetal compromise

o Frequently monitor mother and fetus.

o Administer IV Fluids as prescribed.

o Position on side.

o Administer oxygen by face mask.

o Serves as a guide in determining underlying complications.

o Restores circulating volume to maintain adequate tissue perfusion

o To promote placental perfusion.

o Maximizes available oxygen

o Prepare for emergency delivery, as needed.

for myocardial uptake to reduce cardiac workload and cellular hypoxia.

o Serves as an immediate intervention to prevent complications resulting from hypoxia and fetal death.

HEALTH TEACHINGS

Educate the woman and her family about the etiology and treatment of

placenta previa.

Educate the woman to inform medical personnel about her diagnosis and

no to have vaginal examinations.

If discharged, inform the woman to:

o Avoid intercourse or anything per vagina.

o Limit physical activity.

o Have an accessible person in the event of an emergency.

o Go to the hospital immediately for repeat bleeding or uterine

contractions >6 per hour.

Abruption placenta is the premature separation of the normally

implanted placenta from the uterus. It may be classified as:

o Partial

o Complete

o Marginal

Hemorrhage can be either:

o Occult – the placentaS separates centrally and a large amount of

blood is accumulated under the placenta.

o Apparent – the separation is a long margin and blood flows under

the membranes and through the cervix

PATHOPHYSIOLOGY AND ETIOLOGY

The etiology is unknown.

Women at risk for developing abruption placenta include those with history

of hypertension or previous abruption placenta; those who have rapid

decompression of the uterine cavity, short umbilical cord or presence of a

uterine anomaly or tumor; preterm premature rupture of membranes

(PROM) at <34weeks gestation, increased parity or multiple gestation.

Additional risks occur in existing pregnancies complicated by blunt

abdominal trauma, supine hypotension, PIH, alcohol, cigarette smoking

and cocaine use.

Hemorrhage occurs into the decidua basalis. Then forms a hematoma.

This hematoma can expand as the bleeding increases, causing the

hematoma to increase in size and further detach the placenta from the

uterine wall.

CLINICAL MANIFESTATIONS:

Sudden onset, intense, localized, uterine pain/tenderness with (external)

or without (occult) vaginal bleeding.

Uterine contractions may be low amplitude and high frequency.

FHR may change depending on the degree of hemorrhage; increased

FHR, late decelerations and decreased viability.

Abdominal pain is often present due to increased uterine activity.

Abruptio placenta grades:

o Grade 0 (mild) – small retroplacental clot or small rupture of

marginal sinus; <100 ml blood

o Grade 1 (moderate) – small retroplacental clot; detachment <50%;

>100 ml but <500 ml blood

o Grade 2 (moderate to severe) – significant retroplacental clot;

detachment approaches 50%; blood loss approaches 500 ml

o Grade 5 (moderate to severe) – significant retroplacental clot;

detachment >50%; >500 ml

DIAGNOSTIC EVALUATION

Ultrasound is done but is not always sensitive enough to rule out

diagnosis.

Laboratory screen for APT on mother’s blood to check for fetal

hemoglobin.

MANAGEMENT

This depends on the maternal and fetal status and degree of bleeding.

Mild – conservative management with bed rest, tocolytics and evaluation

of fetus with fetal assessment methods until fetal lung maturity can be

established and delivery accomplished.

Moderate – augment labor if stable and decreased blood loss. Vaginal

delivery is accomplished if cervix dilates. If fetal or maternal status

deteriorates and blood loss excessive, cesarean delivery is performed.

Moderate to severe – restore and maintain maternal physiologic status;

IV/blood replacement.

A pediatric specialty team may be needed at delivery due to prematurity

and other neonatal complications.

COMPLICATIONS

Maternal shock

DIC

Amniotic fluid embolism

Postpartum hemorrhage

Prematurity

Maternal/fetal death

Rapid labor and delivery

NURSING ASSESSMENT

Determine the amount and type of bleeding and the presence or absence

of pain.

Monitor maternal and fetal vital signs.

Palpate the abdomen for contractions.

Measure and record fundal height.

Prepare for possible delivery.

NURSING DIAGNOSIS INTERVENTION RATIONALE

Altered Tissue Perfusion, Placental, related to excessive bleeding causing fetal compromise

o Frequently monitor mother and fetus.

o Administer IV Fluids as prescribed.

o Position on side.

o Administer oxygen by face mask.

o Prepare for emergency delivery, as needed.

o Serves as a guide in determining underlying complications.

o Restores circulating volume to maintain adequate tissue perfusion

o To promote placental perfusion.

o Maximizes available oxygen for myocardial uptake to reduce cardiac workload and cellular hypoxia.

o Serves as an immediate intervention to prevent complications resulting from hypoxia and fetal death.

HEALTH TEACHINGS

Provide information to the woman and her family regarding etiology and

treatment for abruptio placenta.

Encourage involvement from the neonatal team regarding education

related to fetal/neonatal outcome.

Teach high risk women the signs and symptoms of placental abruption

and increased uterine activity.

Instruct woman to report immediately if excessive bleeding and pain occur

at home.

Periodic changes

Periodic changes or fluctuations in FHR occur in response to contractions

and fetal movement and are described in terms of acceleration or deceleration.

Four such responses are acceleration, early deceleration, late deceleration and

variable deceleration. A deceleration (drop) of the fetal heart rate usually

indicates that the fetus is under some sort of stress, which may be a good

healthy sign if it corresponds with movement or uterine contractions, but may be

a bad sign if it happens apart from movement of uterine contractions.

Periodic FHR Changes

Accelerations

Accelerations are transient increases in the FHR (Figure 4). They

are usually associated with fetal movement, vaginal examinations, uterine

contractions, umbilical vein compression, fetal scalp stimulation or even

external acoustic stimulation. The presence of accelerations is considered

a reassuring sign of fetal well-being. An acceleration pattern preceding or

following a variable deceleration (the "shoulders" of the deceleration) is

seen only when the fetus is not hypoxic. Accelerations are the basis for

the nonstress test (NST). The presence of at least two accelerations, each

lasting for 15 or more seconds above baseline and peaking at 15 or more

bpm, in a 20-minute period is considered a reactive NST.

FIGURE 4. Early deceleration in a patient with an unremarkable course of labor. Notice that the onset and the return of the deceleration coincide with the start and the

end of the contraction, giving the characteristic mirror image.

Early Decelerations

Early decelerations are caused by fetal head compression during

uterine contraction, resulting in vagal stimulation and slowing of the heart

rate. This type of deceleration has a uniform shape, with a slow onset that

coincides with the start of the contraction and a slow return to the baseline

that coincides with the end of the contraction. Thus, it has the

characteristic mirror image of the contraction (Figure 5). Although these

decelerations are not associated with fetal distress and thus are

reassuring, they must be carefully differentiated from the other,

nonreassuring decelerations.

FIGURE 5. Nonreassuring pattern of late decelerations with preserved beat-to-beat variability. Note the onset at the peak of the uterine contractions and the return to baseline after the contraction has ended. The second uterine contraction is associated

with a shallow and subtle late deceleration

Late Decelerations

Late decelerations are associated with uteroplacental insufficiency and are

provoked by uterine contractions. Any decrease in uterine blood flow or placental

dysfunction can cause late decelerations. Maternal hypotension and uterine

hyperstimulation may decrease uterine blood flow. Postdate gestation,

preeclampsia, chronic hypertension and diabetes mellitus are among the causes

of placental dysfunction. Other maternal conditions such as acidosis and

hypovolemia associated with diabetic ketoacidosis may lead to a decrease in

uterine blood flow, late decelerations and decreased baseline variability.

A late deceleration is a symmetric fall in the fetal heart rate, beginning at

or after the peak of the uterine contraction and returning to baseline only after the

contraction has ended (Figure 5). The descent and return are gradual and

smooth. Regardless of the depth of the deceleration, all late decelerations are

considered potentially ominous. A pattern of persistent late decelerations is

nonreassuring, and further evaluation of the fetal pH is indicated. Persistent late

decelerations associated with decreased beat-to-beat variability is an ominous

pattern (Figure 6).

FIGURE 6. Late deceleration with loss of variability. This is an ominous pattern, and immediate delivery is indicated.

Variable Decelerations

Variable decelerations are shown by an acute fall in the FHR with a rapid

downslope and a variable recovery phase. They are characteristically variable in

duration, intensity and timing. They resemble the letter "U," "V" or "W" and may

not bear a constant relationship to uterine contractions. They are the most

commonly encountered patterns during labor and occur frequently in patients

who have experienced premature rupture of membranes and decreased amniotic

fluid volume. Variable decelerations are caused by compression of the umbilical

cord. Pressure on the cord initially occludes the umbilical vein, which results in

an acceleration (the shoulder of the deceleration) and indicates a healthy

response. This is followed by occlusion of the umbilical artery, which results in

the sharp downslope. Finally, the recovery phase is due to the relief of the

compression and the sharp return to the baseline, which may be followed by

another healthy brief acceleration or shoulder (Figure 7).

FIGURE 7. Variable deceleration with pre- and post-accelerations ("shoulders"). Fetal heart rate is 150 to 160 beats per minute, and beat-to-beat variability is preserved.

Variable decelerations may be classified according to their depth and

duration as mild, when the depth is above 80 bpm and the duration is less than

30 seconds; moderate, when the depth is between 70 and 80 bpm and the

duration is between 30 and 60 seconds; and severe, when the depth is below 70

bpm and the duration is longer than 60 seconds. Variable decelerations are

generally associated with a favorable outcome. However, a persistent variable

deceleration pattern, if not corrected, may lead to acidosis and fetal distress and

therefore is nonreassuring. Variable decelerations indicating hypoxemia are

shown in Figures 8 and 9. Nonreassuring variable decelerations associated with

the loss of beat-to-beat variability correlate substantially with fetal acidosis and

therefore represent an ominous pattern.

FIGURE 8. Severe variable deceleration with overshoot. However, variability is preserved.

FIGURE 9. Late deceleration related to bigeminal contractions. Beat-to-beat variability is preserved. Note the prolonged contraction pattern with elevated uterine tone between the peaks

of the contractions, causing hyperstimulation and uteroplacental insufficiency. Management should include treatment of the uterine hyperstimulation. This deceleration pattern also may be

interpreted as a variable deceleration with late return to the baseline based on the early onset of the deceleration in relation to the uterine contraction, the presence of an acceleration before the deceleration (the "shoulder") and the relatively sharp descent of the deceleration. However, late decelerations and variable decelerations with late return have the same clinical significance and

represent nonreassuring patterns. This tracing probably represents cord compression and uteroplacental insufficiency.

Pregnancy-Induced Hypertension

Pregnancy-induced hypertension (PIH) is a form of high blood pressure in

pregnancy and excess protein in the urine after 20 weeks of pregnancy. It occurs

in about 5 percent to 8 percent of all pregnancies. Pregnancy-induced

hypertension is also called preeclampsia. Originally it was called toxemia

because researchers pictured a toxin of some kind being produced by the

woman in response to the foreign protein of the growing fetus, the toxin leading

to the typical symptoms. No such toxin has ever been identified. It occurs most

often in young women with a first pregnancy.

Sign and symptoms

Usually, there are three primary characteristics of this condition, including the

following:

high blood pressure (a blood pressure reading higher than 140/90 mm Hg,

or a significant increase in one or both pressures)

proteinuria (protein in the urine)

edema (swelling)

Other signs and symptoms of preeclampsia — which can develop gradually or

strike suddenly, often in the last few weeks of pregnancy — may include:

Severe headaches

Changes in vision, including temporary loss of vision, blurred vision or

light sensitivity

Upper abdominal pain, usually under the ribs on the right side

Nausea or vomiting

Dizziness

Decreased urine output

Sudden weight gain, typically more than 2 pounds a week.

Pathophysiology Events

Vasospasm

Interstitial effects

Vasoconstriction Decreased glomeruli filtration rate and

increased permeability of glomeruli membranes

Poor organ perfusion

Increased serum blood urea nitrogen, uric acid,

and creatinine

Diffusion of fluid from blood stream into interstitial tissue

EdemaIncreased blood pressure

Decreased urine output and proteinuria

Vascular effects Kidney effects

Causes

The cause of PIH is unknown. Some conditions may increase the risk of

developing PIH, including the following:

pre-existing hypertension (high blood pressure)

kidney disease

diabetes

PIH with a previous pregnancy

mother's age younger than 20 or older than 40

multiple fetuses (twins, triplets)

Classification

PIH is classified as gestational hypertension, mild preeclampsia, severe

preeclampsia, and eclampsia, depending on how far advanced it has become.

Gestational Hypertension

A woman is said to have gestational hypertension when she

develops an elevated blood pressure (140/90 mmHg) but has no

proteinuria or edema.

Mild Preeclampsia

A woman is said to be mildly preeclamptic when her blood pressure

rises to 140/ 90 mmHg, taken on two occasions at least 6 hours apart.

With mild preeclampsia, in addition to the hypertension the woman has

proteinuria ( 1+ or 2+ on a reagent test strip on a random sample). Edema

also may present. This develops, as mentioned, because of the protein

loss, sodium retention, and lowered glomerular filtration rate. Edema

begins to accumulate in the upper part of the body, rather than just the

ankle edema of pregnancy. A weight gain of more than 2lb/wk in the

second trimester or 1lb/wk in the third trimester usually indicates abnormal

tissue fluid retention.

Severe Preeclampsia

A woman has passed from mild to severe preeclampsia when her

blood pressure has risen to 160/110 mmHg or above on at least two

occasions 6 hours apart at bed rest or her diastolic pressure is 30 mm Hg

above the prepregnancy level. Marked proteinuria, 3+ or 4+ on a random

urine sample or more than 5g in a 24-hour sample, and extensive edema

are also present.

Eclampsia

This is most severe classification of hypertension of pregnancy.

Convulsion or coma accompanied by signs and symptoms of

preeclampsia.

Nursing Management

Nursing Diagnosis Intervention Rationale1. Fluid volume

deficient related to altered intake during labor.

a. Monitor vital signs every hour.

b. Monitor intake and output strictly; notify health care provider if urine output is less than 30ml/hour.

c. Position the patient on her left side

d. If urine output is reduced, carefully assess the patient for peripheral edema, hyperreflexia, increased blood pressure, and presence of urine protein.

a. With PIH, increased blood pressure may occur.

b. These measures help ensure adequate hydration.

c. To aid kidney perfusion and increase cardiac and urine output.

d. Decreased urine output, increased blood pressure, hyperreflexia, and peripheral edema may indicate intrapartal PIH. Proteinuria may result from dehydration, exhaustion, or preeclampsia.

2. Ineffective tissue perfusion: fetal cardiac and cerebral related to altered placental blood flow caused by vasospasm and thrombosis.

a. Position to side

b. Monitor fetal activity

c. Evaluate NST

d. Increased protein intake

a. To promote placental perfusion

c. To determine fetal status

d. To replace protein lost through kidneys.

Medical Management

Drugs used in pregnany-induced hypertension

Hydralazine and Labetalol- hypotensive drug to reduce hypertension.

These drugs act to lower blood pressure by peripheral dilatation without

interfering with placental circulation.

Magnesium Sulfate- drug of choice to prevent eclampsia. It acts as

anticonvulsant.

Cathartic- reduces edema by causing a shift in fluid from the extracellular

spaces into the intestine. It has a central nervous system depressant

action which lessens the possibility of seizures.

Calcium gluconate- antidote for magnesium toxicity.

Multiple births occur when multiple fetuses are carried during one

pregnancy. Since 1970, the prevalence of multiple births has been increasing

because of more widespread use of assisted reproductive technologies to treat

infertility. Multifetal pregnancies are high-risk pregnancies with numerous

associated fetal and neonatal complications. Researchers have studied twins in

an attempt to separate the influence of genetic and environmental factors on both

fetal and postpartum development.

Pathophysiology

Multiple births include twins and higher-order multiples (eg, triplets,

quadruplets). The 2 types of twins are monozygotic and dizygotic.

Dizygotic twins, which sometimes are called fraternal twins, are produced

when 2 sperm fertilize 2 ova. Separate amnions, chorions, and placentas are

formed in dizygotic twins (see Media file 1). The placentas in dizygotic twins may

fuse if the implantation sites are proximate. The fused placentas can be easily

separated after birth.

Monozygotic twins develop when a single fertilized ovum splits during the

first 2 weeks after conception. Monozygotic twins are also called identical twins.

An early splitting (ie, within the first 2 d after fertilization) of monozygotic twins

produces separate chorions and amnions (see Media file 1). These dichorionic

twins have different placentas that can be separate or fused. Approximately 30%

of monozygotic twins have dichorionic/diamniotic placentas.

Later splitting (ie, 3-8 d after fertilization) results in

monochorionic/diamniotic placentation (see Media file 2). Approximately 70% of

monozygotic twins are monochorionic/diamniotic. If splitting occurs even later (ie,

during 9-12 d after fertilization), monochorionic/monoamniotic placentation

occurs (see Media file 3). Monochorionic/monoamniotic twins are rare; only 1%

of monozygotic twins have this form of placentation.

Monochorionic/monoamniotic twins have a common placenta with vascular

communications between the 2 circulations. These twins can develop twin-to-twin

transfusion syndrome (TTTS). If twinning occurs more than 12 days after

fertilization, then the monozygotic pair only partially split, resulting in conjoined

twins.

Triplets can be monozygotic, dizygotic, or trizygotic. Trizygotic triplets

occur when 3 sperm fertilize 3 ova. Dizygotic triplets develop from one set of

monozygotic cotriplets and a third cotriplet derived from a different zygote.

Finally, 2 consecutive zygotic splittings with one split results in a vanished fetus

and monozygotic triplets.

Although the evaluation of the placenta or placentas after the birth is

important in all multifetal pregnancies, the examination may not always help

determine zygosity, as in the case of monozygotic twins, in which 30% have a

dichorionic/diamniotic placentation.

Etiology

Mortality/Morbidity

Multifetal pregnancies are high-risk pregnancies. The fetal mortality rate

for twins is 4 times the fetal mortality rate for single births. The neonatal mortality

rate for twins is more than 5 times greater than the neonatal mortality rate for

single births. Higher-order multiple births have even greater mortality rates than

twin and single births.

A high prevalence of low birth weight infants, due to prematurity and

intrauterine growth retardation (IUGR) and their associated complications,

contribute to this problem. Twins have increased frequency of congenital

anomalies, placenta previa, abruptio placenta, preeclampsia, cord accidents, and

malpresentations, as well as asphyxia/perinatal depression, group B

streptococcal (GBS) infections, hyaline membrane disease (HMD), and TTTS.

Race

The frequency of naturally occurring twin births varies by race. Black

women have the highest birth rate of twins, followed by white and Hispanic

women. Asian women have the lowest birth rate of twins. A racial disparity

between black and white twin stillbirths is observed in the United States. Risk of

stillbirth is elevated in black fetuses compared with white fetuses among twins

but not among triplets.

Age

Maternal age has no effect on monozygotic twin births. Advanced

maternal age (>35 y) is associated with increased risk of dizygotic twins.

Prevalence of naturally occurring twin births has increased recently because of

the trend to delay childbearing to later years.

CLINICAL

History

Most multifetal pregnancies are prenatally diagnosed. Maternal complaints

of excessive weight gain, hyperemesis gravidarum, and/or sensation of more

than one moving fetus; use of ovulation-inducing drugs; or family history of

dizygotic twins should alert caregivers to the possibility of a multifetal pregnancy.

Physical

Women with multifetal pregnancies may have a uterine size that is

inconsistently large for dates and may experience accelerated weight gain. Upon

auscultation, more than one fetal heart rate may be heard.

Causes

Risk factors for multifetal pregnancy can be divided into natural and

induced. Risk factors for natural multifetal pregnancy include advanced maternal

age, family history of dizygotic twins, and race. Induced multifetal pregnancies

occur following infertility treatment via the use of ovulation-inducing agents or

gamete/zygote transfer.

WORKUP

Lab Studies

CBC count: In TTTS, the donor twin is frequently anemic at birth. The

recipient twin is polycythemic at birth.

Calcium level: Hypocalcemia is common in premature infants, especially

the donor twin in TTTS.

Glucose level: Hypoglycemia is common in premature infants, especially if

TTTS is present.

Bilirubin level: Hyperbilirubinemia due to TTTS may develop in

polycythemic infants.

Imaging Studies

Maternal ultrasonography: This study confirms most multifetal

pregnancies.

Neonatal head ultrasonography: Premature infants from multifetal

pregnancies have a higher incidence of intraventricular hemorrhage and

periventricular leukomalacia than singleton infants of the same gestational

age.

TREATMENT

Medical Care

Medical care of the woman with multifetal pregnancy is beyond the scope

of this article.

The specific medical care required by infants from multifetal births varies

and is dictated by whatever complications may be present. Many require

only routine newborn care, whereas those with significant prematurity or

other complications may require high-level intensive care in specialized

centers.

The usual method of delivery for higher-order multiple births (eg, triplets,

quadruplets) is cesarean delivery. Cesarean delivery is also the usual

method of delivery for twins in the following situations:

o Breech/vertex presentation with the possibility of interlocking twins

o Monoamniotic twins

o Conjoined twins

o Congenital anomalies that threaten increased neonatal morbidity in

a twin

o Delayed interval delivery: Delayed interval delivery of remaining

fetuses in multifetal pregnancies at the border of viability is

becoming more common. Before 30 weeks’ gestation, delayed

delivery for 2 or more days is associated with improved survival in

the second twin.

Delivery room management of infants from multifetal pregnancies requires

adequate personnel skilled in neonatal resuscitation. Infants from

multifetal pregnancies are at increased risk of birth asphyxia and

respiratory distress syndrome (RDS). Such infants may require bag mask

ventilation and endotracheal intubation in the delivery room.

Partial exchange transfusion may be necessary in donor or recipient twins

from TTTS.

o Partial exchange transfusions are used to increase hemoglobin

concentrations in anemic donor twins while maintaining euvolemia.

Small aliquots (5-15 mL) of packed RBCs are infused (usually via

an umbilical venous catheter) following removal of an equal volume

of the infant's blood until a desired hemoglobin is attained. The

transfused packed RBCs should be appropriately cross-matched,

cytomegalovirus (CMV) negative, and irradiated.

o Partial exchange transfusions are used to decrease hemoglobin

concentrations in polycythemic recipient twins while maintaining

euvolemia. Small aliquots (5-10 mL) of either a colloid such as

fresh frozen plasma or a crystalloid such as a 0.9% saline solution

are infused (usually via an umbilical venous catheter) following

removal of an equal volume of the infant's blood until a desired

hemoglobin level is attained.

Consultations

A woman with multiple gestation pregnancy may benefit from a

consultation with a perinatologist. A neonatologist may be involved in the

postnatal care of multiple birth infants, particularly if the births are premature or if

congenital anomalies are present.

MEDICATION

Medication requirements vary depending on specific comorbidities. Refer

to the eMedicine topics for the specific complication.

FOLLOW-UP

Complications

Prematurity: Infants from multifetal pregnancies are more likely to be born

prematurely and are more likely to require neonatal intensive care.

Approximately 50% of twin deliveries occur before 37 weeks' gestation.

The length of gestation inversely decreases with the number of fetuses

present. Infants from multifetal pregnancies represent 20% of very low

birth weight infants.

Hyaline membrane disease: Twins born at fewer than 35 weeks' gestation

are twice as likely to develop HMD as single birth infants born at fewer

than 35 weeks' gestation. The prevalence of HMD is greater in

monozygotic twins than in dizygotic twins. The concordance rate for HMD

(ie, both twins have HMD) is greater in monozygotic twins than in dizygotic

twins. If only one of a pair of twins develops HMD, then the second twin is

more likely to develop HMD than the first twin.

Birth asphyxia/perinatal depression: Newborns from multifetal pregnancies

have an increased frequency of perinatal depression and birth asphyxia

due to various causes. Umbilical cord entanglement, locked twins, a

prolapsed umbilical cord, placenta previa, and uterine rupture can occur

and result in asphyxiation of an infant. Cerebral palsy is 6 times more

common in twin births and 30 times more common in triplet births than in

single births. Monochorionic/monoamniotic twins are at highest risk for

cord entanglement. The second-born twin is at greatest risk for birth

asphyxia/perinatal depression.

Group B streptococcal infections: Early onset GBS infections in low birth

weight infants are nearly 5-fold greater than in average weight singletons.

Vanishing twin syndrome: Early ultrasonography diagnosis has revealed

that as many as one half of all twin pregnancies result in the delivery of

only a single fetus; the second twin vanishes. Intrauterine demise of one

twin can result in neurologic sequelae in the surviving twin. Acute

exsanguination of the surviving twin into the relaxed circulation of the

deceased twin can result in intrauterine CNS ischemia.

Congenital anomalies, acardia, twin reversed arterial perfusion sequence:

Congenital anomalies are more common in twins than in a single fetus.

CNS, cardiovascular, and GI defects occur with increased frequency.

Monozygotic twins have increased prevalence of deformations secondary

to intrauterine space constraints. Common deformations in twins include

limb defects, plagiocephaly, facial asymmetry, and torticollis. Acardia is a

rare anomaly unique to multifetal pregnancy. In this condition, one twin

has an absent or rudimentary heart. Twin reversed arterial perfusion

(TRAP) sequence occurs when an acardiac twin receives all of the blood

supply from the normal "pump" twin. This only occurs in monochorionic

twins. Blood enters the acardiac twin in a reversed perfusion manner.

Blood enters this fetus via an umbilical artery and exits via the umbilical

vein. The excessive demands on the normal "pump" twin can cause

cardiac failure in that twin.

TTTS: This syndrome occurs in monochorionic/monoamniotic or

monochorionic/diamniotic twins. Vascular anastomoses in the

monochorionic placenta result in transfusion of blood from one twin (ie,

donor) to the other twin (ie, recipient). Polyhydramnios develops in the sac

of the recipient twin because of volume overload and increased fetal urine

output. Oligohydramnios develops in the sac of the donor twin because of

hypovolemia and decreased urine output. Severe oligohydramnios can

result in the stuck twin phenomena, in which the twin appears in a fixed

position against the uterine wall.

Conjoined twins

Incomplete late division of monozygotic twins produces conjoined

twins.

Conjoined twins are connected at identical points and are classified

according to site of union, as follows:

Thoracopagus - Joined at chest (40%)

Xiphopagus/omphalopagus - Joined at abdomen (34%)

Pygopagus - Joined at buttocks (18%) 

Ischiopagus - Joined at ischium (6%) 

Craniopagus - Joined at head (2%)

IUGR: The birth weights are smaller in infants from multifetal pregnancies

than weights in corresponding singletons. However, when combined, birth

weights of twins are greater than weights of corresponding singletons.

Most of the deficit of birth weight occurs in the final 8-11 weeks of

pregnancy. Average birth weights are similar between twins and

singletons until 32 weeks’ gestation. Average birth weights are similar

between triplets and singletons until 29 weeks’ gestation. Birth weight

discrepancies of more than 20-25% are considered discordant. Discordant

birth weights occur in 10% of twins. The cause of discordant birth weight

among twins is the difference between each twin's placental surface area

or TTTS. Discordant birth weights among triplets are more common than

discordant birth weights between twins. Approximately 30% of

pregnancies with triplets have a birth weight discordance of more than

25%.

Prognosis

The prognosis of infants born from multifetal pregnancies depends on the

complications that develop. Some studies have reported that the risks of death,

chronic lung disease, and grade III/IV intracranial hemorrhage were similar in

twins and singletons. Other studies have reported a higher prevalence of

complications such as necrotizing enterocolitis, retinopathy of prematurity, and

patent ductus arteriosus in infants from multifetal pregnancies versus singletons.

MISCELLANEOUS

Medical/Legal Pitfalls

Most problems that could result in medical legal action against the health

professional involve prenatal and intrapartum care issues.

Special Concerns

Multiple births have significant economic implications. Twins and triplets

have more frequent and longer duration hospitalizations than singletons.

Multiple births contribute disproportionately to inpatient hospital costs in

the first 5 years of life.

MULTIMEDIA

Diamniotic/dichorionic placentation.

Diamniotic/monochorionic placentation.

Monoamniotic/monoamniotic placentation.

Preliminary Signs of LaborPreliminary Signs of Labor

Before labor, a woman often experiences subtle signs that signal the

onset of labor. All pregnant women should be taught these signs so that they can

recognize when labor is beginning.

Lightening

This changes a woman’s abdominal contour, because the uterus

becomes lower and more anterior. Lightening gives a woman relief from a

diaphragmatic pressure and shortness of breath that she has been

experiencing and in this way “lightens” her load. As the fetus sinks lower in

the pelvis, the mother may experience shooting leg pains from the

increased pressure on the sciatic nerve, increased amounts of vaginal

discharge, and urinary frequency from pressure on the bladder.

Increased in Level of Activity

A woman may awaken on the morning of labor full of energy, in

contrast to her feelings of chronic fatigue during the previous month. This

increase in activity is related to an increase in epinephrine release that is

initiated by a decrease in progesterone produced by the placenta.

Additional epinephrine prepares a woman’s body for the work of labor

ahead.

Braxton Hicks Contractions

Also known as false labor or practice contractions. Braxton Hicks

are sporadic uterine contractions that actually start at about 6 weeks,

although one will not feel them that early. Most women start feeling them

during the second or third trimester of pregnancy. Braxton Hicks

contractions are a tightening of the uterine muscles for one to two minutes

and is thought to be an aid to the body in its preparation for birth. Not all

expectant mothers have these contractions. They are thought to be part of

the process of effacement, the thinning and dilation of the cervix.

Ripening of the Cervix

Ripening of the cervix is an internal sign seen only on pelvic

examination. Throughout pregnancy, the cervix feels soften that normal,

similar to the consistency of an earlobe (Goodell’s sign) at term, the cervix

becomes still softer, and it tips forward. Ripening is an internal

announcement that labor is very close at hand.

Signs of True LaborSigns of True Labor

Signs of true labor involve uterine and cervical changes. The more a

woman knows about true labor signs, the better, because then she will be better

able to recognize them. This is helpful both to prevent preterm birth and for the

woman to feel secure knowing what is happening during labor.

Uterine Contractions

The surest sign that labor begun is productive uterine contractions.

Because contractions are involuntary and come without warning, their

intensity can be frightening in early labor.

Show

As the cervix softens and ripens, the mucus plug that filled the

cervical canal during pregnancy (operculum) is expelled. The exposed

cervical capillaries leak blood as a result of pressure exerted by the fetus.

The blood, mixed with mucus, takes on a pink tinge and is referred to as

“show” or “bloody show.”

Rupture of Membranes

Labor may begin with rupture of the membranes, experienced

either as a sudden gush or as scanty, slow seeping of clear fluid from the

vagina. Early rupture of membranes can be advantageous if it causes the

fetal head to settle closely into the pelvis, this can actually shorten labor.

Two risks associated with ruptured membranes are intrauterine

infection and prolapse of the umbilical cord, which can cut off the oxygen

supply to the fetus.

DIFFERENTIATION BETWEEN TRUEDIFFERENTIATION BETWEEN TRUEAND FALSE LABOR CONTRACTIONSAND FALSE LABOR CONTRACTIONS

Type of Change True Labor False Labor

Timing of

Contractions

Occur at regular

intervals.

Interval between

contraction decreases.

Increase in

duration, frequency

and intensity.

Often occur at irregular

intervals.

Interval between

contractions remains

the same or increases.

Do not increase in

duration, frequency

and intensity.

Location of Contractions Felt first in the lower

back and sweep

around to the

abdomen in wave

Felt first abdominally

and remain confined to

the abdomen and

groin.

Change with movement Generally intensified

by walking.

Continue regardless of

a woman’s level of

activity.

Generally unaffected

by walking.

Often disappear with

ambulation and sleep

Effects on the Cervix Results in progressive

cervical dilatation and

effacement

Do not result in

cervical dilatation and

effacement.

Response to Sedation Not affected by mild

sedation.

Generally relieved by

mild sedation

BIBLIOGRAPHY

Book Sources:

Pillitteri, Adele. Maternal and Child Health Nursing: Care for the Childrearing and Childbearing Family. 4th Edition. Volume 1.

Smeltzer, Suzanne and Brenda Bare. Textbook of Medical-Surgical Nursing. 10th Edition.

Williams and Wilkins. The Lippincott: Manual of Nursing Practice. 8th Edition. Page 1174 – 1269.

Internet Sources:

http://www.emedicine.com/ped/TOPIC2599.HTM

http://www.fetalmonitorstrips.com/learn_more.html

http://www.moondragon.org/pregnancy/truefalselabor.html

http://www.riverwalk-obgyn.com/obcorner/tflabor.html